Stress proteins, arthritis, and autoimmunity.
Stress proteins, arthritis, and autoimmunity.
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应激蛋白、关节炎和自身免疫。
DOI：
10.1002/anr.1780321202
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发表时间：
1989
影响因子：
--
通讯作者：
Winfield,JB
中科院分区：
文献类型：
--
作者：
Winfield,JB
应激蛋白在进化过程中高度保守，不仅是因为它们在细胞对应激攻击的反应中具有重要的基础作用，而且还因为它们在细胞活化和细胞生长、蛋白质功能调节、蛋白质运输和蛋白质组装中起着关键作用。目前，对应激蛋白的基本细胞生物学的研究非常激烈，并且在未来一段时间内肯定会持续下去。免疫学家和风湿病学家特别感兴趣的是几个领域的数据汇集，这些数据表明，通常感染人类的微生物中的应激蛋白可能是体液和细胞自身免疫反应以及随后的显性自身免疫疾病表达的触发因素。因此，结核分枝杆菌和其他细菌的应激蛋白与哺乳动物的应激蛋白有密切的同源性，可能参与了佐剂诱导的大鼠关节炎的发病机制，也可能参与了人类RA和反应性关节炎的发病机制。在这个领域还有大量的工作要做，包括(A)产生和繁殖特异性反应性T细胞克隆，(b)微生物应激蛋白和宿主蛋白共享的免疫识别元件和关键表位的分子描述，(c)定义α - β和γ - δ tcr对T细胞对应激蛋白反应性的相对贡献，以及(d)澄清使T细胞对应激蛋白产生持续自身反应的环境。然而，手头的数据足够令人信服，表明针对识别应激蛋白的T细胞的疫苗接种可能最终成为我们治疗手段的一部分，以预防或治疗某些形式的关节炎。（摘要删节250字）
Stress proteins have been highly conserved during evolution not only because of their fundamental importance in the response of the cell to stressful assaults, but also because they have critical roles in cellular activation and cell growth, regulation of protein function, protein transport, and protein assembly. Research focusing on the basic cell biology of stress proteins is intense at present, and will surely continue to be for some time to come. Of particular interest to immunologists and rheumatologists is the convergence of data in several fields that suggest that stress proteins in microorganisms that commonly infect humans may be triggers of humoral and cellular autoimmune responses and consequent overt autoimmune disease expression. Thus, stress proteins of M tuberculosis and other bacteria are close homologs of stress proteins in mammals, and may be involved in the pathogenesis of adjuvant-induced arthritis in rats and, possibly, of RA and reactive arthritis in humans. A great deal of work remains to be done in this area, including (a) generation and propagation of specifically reactive T cell clones,(b) molecular delineation of the immune recognition elements and critical epitopes shared by microbial stress proteins and host proteins,(c) definition of the relative contribution of alpha beta and gamma delta TCRs to T cell reactivity to stress proteins, and (d) clarification of the circumstances that enable persistent T cell autoreactivity to stress proteins. The data at hand are sufficiently compelling, however, to suggest that vaccination against T cells that recognize stress proteins may eventually become part of our therapeutic armamentarium to prevent or cure some forms of arthritis.(ABSTRACT TRUNCATED AT 250 WORDS)